1. Technical Field of the Invention
The present invention relates to novel cosmetic/pharmaceutical compositions containing an effective amount of at least one extract of at least one Iridaceae, for loosening and/or relaxing the cutaneous and/or subcutaneous tissue, especially for treating (reducing or eliminating) normal and small (fine) skin wrinkles.
2. Description of the Prior Art
Women, or even men, today seek to maintain a youthful appearance for as long as possible and, consequently, seek to attenuate the signs of skin aging, which manifest themselves especially by normal and small wrinkles. In this regard, advertisements and fashion promote products intended to maintain a radiant skin for as long as possible and without wrinkles, which is the sign of a youthful skin, all the more so since physical appearance is important for peace of mind and/or for morale. Thus, it is important to feel physically and spiritually young.
To date, normal and small wrinkles were treated with cosmetic products containing active agents acting on the skin, for example by moisturizing it or by enhancing its cellular renewal or by promoting the synthesis of collagen which constitutes the cutaneous tissue. However, also to date, it was not known to this art how to treat wrinkles by acting on the muscular elements present in the skin.
It is known that the facial platysma muscles are under the control of the motor nerve afferences of the facial nerve and that, moreover, the interlobular septa of the hypodermis contain therein fibers which constitute a striated muscular tissue (panniculus carnosus). Too, it is also known that a subpopulation of fibroblasts of the dermis, designated myofibroblasts, exhibits characteristics which are common with the muscular tissue.
Prologue:
In the laboratories of the assignee hereof, in certain pathological and therapeutic conditions, the influence exerted on facial wrinkles by the nerves controlling all of this muscular tissue has been observed. Thus, in facial nerve conditions, in which the transmission of the nerve impulse is interrupted and/or reduced, there is observed in the area of innervation a paralysis of the facial muscles. This facial paralysis results, besides other clinical signs, in an attenuation, or even disappearance of the wrinkles.
In contrast, in the states of facial muscular hypercontraction, accentuation of facial wrinkles has also been observed. Furthermore, an accentuation of the facial wrinkles in the muscular hypertonia states in Parkinson's disease and side effects induced by neuroleptics too has been observed.
Moreover, it has been demonstrated that the botulinus toxin, originally used for treating spasms, is active on muscular spasticity states (see A. Blitzer et al., Arch. Otolaryngol. Head Neck Surg., 119, pages 1018 to 1022 (1993)) and on the wrinkles on the glabella which are intersuperciliary wrinkles (see J. D. Carruters et al., J. Dermatol. Surg. Oncol., 18, pages 17 to 21 (1992)). Consequently, it is possible to influence, via a pharmacological action, the nervous component of the wrinkles.
In the peripheral nervous system, the junction between a nerve and a muscle constitutes the neuromuscular plate, upstream of which there is the afferent nerve route denominated "motoneuron."Moreover, the cellular membranes of each nerve fiber comprise numerous ion channels, and especially chlorine channels, capable of permitting the corresponding element in ionic form, and in the case of the chlorine channels in chloride form, to pass therethrough. These channels are associated with neuronal receptors. The neuronal receptors associated at the periphery with the chlorine channels are especially receptors for glycine (glycine-strychnine sensitive receptors) and receptors for type A GABA (GABA-A receptors) (GABA=.gamma.-aminobutyric acid).
It too is known that it is possible to reduce the excitability of the motoneuron by various pharmacological agents acting on the glycine-strychnine sensitive receptors or on the GABA-A receptors of the peripheral nervous system (see W. Sieghart, Trends in Pharmacological Science, December 1992, Vol. 131, pages 446 to 450). Thus, it is possible to modulate the excitability of the motoneuron, for example by glycine or gamma-aminobutyric acid (GABA).
The activation of these receptors opens the chlorine channels and permits entry of chloride ions, which results in an increase in the chloride ions in the cells of the nerve fiber and therefore to a hyperpolarization of the motoneurons which become, as a result, less excitable. This reduction in excitability of the motoneuron causes a lesser stimulation of the muscle fiber, thereby effecting its loosening.